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At least 1,117 records · Page 62Linked to original sources
PubMed1990

Clinical and hematological improvement in a patient receiving danazol therapy for myelofibrosis with myeloid metaplasia.

We report the positive effect of danazol on clinical and hematological data in a patient with myelofibrosis and myeloid metaplasia. Severe cytopenia was corrected within 2 months and was maintained for an additional 2-month period. Myeloid metaplasia (lymph nodes and skin lesions) was greatly reduced. The patient experienced no side effects. We propose further trials to confirm the utility of this agent in this disease.

Danazol↗
PubMed1989

Increased circulating CSF-1 (M-CSF) in myeloproliferative disease: association with myeloid metaplasia and peripheral bone marrow extension.

Myeloproliferative disease (MPD) is heterogeneous in phenotypic expression and may display features consistent with expansion and activation of the monocyte/macrophage population during its course. The role of colony-stimulating factor-1 (CSF-1) in the pathophysiology of MPD was investigated by measuring circulating CSF-1 levels and examining their relationship to disease phenotype. Serum CSF-1 concentrations, measured by radioimmunoassay, were elevated in all MPD phenotypes. CSF-1 levels differed significantly between groups of patients with essential thrombocythemia, polycythemia vera, and postpolycythemic or agnogenic myeloid metaplasia (in ascending order). CSF-1 serum levels were positively correlated with spleen size and the degree of peripheral bone marrow extension, determined by scintigraphy using a macrophage-seeking isotope. There was no correlation between CSF-1 concentration and circulating levels of erythrocytes, neutrophils or platelets, or the presence of bone marrow fibrosis. Elevated serum CSF-1 levels appear to be associated with an expanded monocyte/macrophage population in MPD. In view of the known cooperativity between CSF-1 and other growth factors in regulating hematopoiesis, the finding of increased serum CSF-1 concentrations and its association with myeloid metaplasia and bone marrow extension may indicate a pathophysiologic role for CSF-1 in determining the phenotypic expression of MPD.

Bone Marrow↗
PubMed1977

[Cytological detection of a myeloic metaplasia in punctates of transplanted kidneys and their diagnostic importance (author's transl)].

In 30 patients who had undergone renal transplantations, 45 renal biopsies were carried through for a suspected acute immuno-incompatibility (rejection) during the period from 1974-1975. Of all bioptic material taken swab-preparations were made at the same time, aiming at clarifying the cytomorphological criteria of the acute transplant rejection. In 14 out of 27 cases where an acute transplant rejection was histologically diagnosed, myelocytes and normoblasts were found in the smears. In one out of two chronic cases of transplant rejection the detection of metaplasias was negative. Thus, the detection of myeloic metaplasias in renal punctates is an important criterium for the cytodiagnostics of a transplant rejection crisis.

Biopsy, Needle↗
PubMed1986

Ultrastructure of sinusoids in patients with agnogenic myeloid metaplasia.

Four patients with agnogenic myeloid metaplasia underwent liver biopsies. Under light microscopy, sinusoidal infiltration was very mild or moderate, liver architecture was normal with sinusoids slightly dilated and the perisinusoidal collagen network was increased. Under electron microscopy, in perfusion-fixed sinusoids, the following abnormalities were noticed. a) Presence of hemopoietic cells (erythroid, megakaryocytic, lymphoid, myeloid) at different stages of maturation. More frequently observed in the lumen than in the Disse space, they were usually isolated and never exceeded 2 or 3 cells. In the Disse space, hepatocytes in contact with hemopoietic cells were devoid of microvilli. In the lumen they were close to endothelial cells and Kupffer cells. Kupffer cells were numerous with intense phagocytic activity. b) Numerous collagen bundles encircling sinusoids. c) Transformation of perisinusoidal cells into transitional cells with few lipids, prominent RER, long and thick processes containing filaments sometimes condensed below the plasma membrane. Although only one patient showed clinical evidence of portal hypertension of sinusoidal origin, these results suggest that hepatic vascular resistance might be raised in agnogenic myeloid metaplasia.

Cell Adhesion↗
PubMed1979

Agnogenic myeloid metaplasia and spinal cord compression.

A 55-year-old White male with agnogenic myeloid metaplasia, proved on bone marrow trephine biopsy, underwent splenectomy for abdominal discomfort. Six months later he developed paraparesis and on myelography multiple extradural obstructions were seen. In the absence of other obvious diagnostic possibilities, these were attributed to areas of extramedullary haematopoiesis, and he was treated with local radiotherapy. However, the neurological deficit progressed and emergency laminectomy and decompression were undertaken. Tissue obtained at this time confirmed the diagnosis of agnogenic myeloid metaplasia. A repeat myelogram showed complete relief of the obstruction, but the patient developed fulminating septicaemia and died. These findings are reported in view of the great rarity of spinal cord compression due to multiple areas of extramedullary haematopoiesis.

Humans↗
PubMed1983

Barrett's metaplasia and dysplasia in postmyotomy achalasia patients.

Three patients who were 8 to 30 years status postmyotomy for achalasia were shown to develop Barrett's columnar metaplasia of the esophagus. In one instance, the patient had multiple areas of severe dysplasia to carcinoma in situ. There have been only a few reports in the world literature of Barrett's metaplasia occurring in postmyotomy achalasia patients. Our experience would indicate it may be a more common complication than previously appreciated. Also, a possible causal relationship between surgical intervention, Barrett's epithelium, and adenocarcinoma in achalasia is suggested.

Adenocarcinoma↗
PubMed1981

Spontaneous "remission' of agnogenic myeloid metaplasia and termination in acute myeloid leukemia.

Acute myeloid leukemia developed in two men with well-documented agnogenic myeloid metaplasia 49 and 27 months, respectively, after initial diagnosis. Both men had spontaneous hematologic remissions of myeloid metaplasia 22 and 16 months prior to leukemic transformation. Neither patient received any precedent radiation or cytotoxic chemotherapy. The remissions and subsequent transformation to acute leukemia were documented by bone marrow aspiration, biopsy, and reticuloendothelial marrow scans, as well as in vitro cell cultures and cytogenetic study. A review of the literature revealed nine other patients who had conversion to acute leukemia in the absence of preceding radiation or cytotoxic chemotherapy. However, the hematologic remission prior to transformation to leukemia.

Bone Marrow↗
PubMed1982

Splenectomy for agnogenic myeloid metaplasia.

Only a fraction of the patients with myeloid metaplasia have indications for splenectomy develop. Palliation for symptomatic splenomegaly is highly successful. Significant relief from hypersplenism, anemia or thrombocytopenia was achieved, however, in less than half of the patients. Since patients with severe thrombocytopenia are at continuing risk of spontaneous hemorrhage and of bleeding after minor trauma, splenectomy appears to be justified in these patients, provided that studies of peripheral blood and bone marrow have excluded those with leukemic conversion. The benefit obtained from splenectomy in patients with chronic anemia requiring frequent transfusions in less certain, particularly in men and in patients converting to myeloid metaplasia from polycythemia vera. In some instances, the continuation of transfusions may result in less morbidity and better palliation than operation. Although the course of this myeloproliferative disorder from first symptoms to death frequently extends for more than a decade, the manifestations which may provide an indication for splenectomy usually occur late in the course of the disease. The element as well as the morbidity of the operation makes a thorough evaluation of each patients essential before splenectomy is considered.

Adult↗
PubMed1982

Mechanism of extramedullary haematopoiesis in rabbits with saponin-induced myelofibrosis and myeloid metaplasia.

The saponin-induced myelofibrosis and myeloid metaplasia model in the rabbit was used to study mechanisms of extramedullary haematopoiesis. Haematopoietic progenitor cells, erythroid colony forming units (CFU-E) and burst forming units (BFU-E) were assayed serially in the peripheral blood, spleen and bone marrow after saponin administration, employing the in vitro methylcellulose culture technique. Animals that had undergone splenectomy prior to saponin administration were also studied. The results demonstrated increases of progenitor cells in the blood and spleen and a simultaneous depletion of such cells in marrow after saponin treatment. The results in splenectomized animals were similar to those observed in non-splenectomized animals after saponin administration. The findings indicate that following saponin administration there is a release of CFU-E and BFU-E from bone marrow into periphery and probably deposition in the spleen, and suggest that myeloid metaplasia in myelofibrosis may result from colonization of extramedullary sites originating from the bone marrow.

Animals↗
PubMed1981

[Two cases of agnogenic myeloid metaplasia associated with chronic lymphocytic leukemia (author's transl)].

Two cases of agnogenic myeloid metaplasia associated with chronic lymphocytic leukemia are reported. Both cases are documented by clinic, bone marrow biopsy, immunologic and isotopic studies. Such observations allow to point out the lymphoproliferative pattern that can be found among any agnogenic myeloid metaplasia. It is suggested that this disease includes a monoclonal lymphoid proliferation which may become the prevailing symptom.

Aged↗
PubMed1978

[Suppression of hepatic myeloid metaplasia after irradiation of the spleen in a case of spent polycythemia (author's transl)].

In a case of spent polycythemia after irradiation of the spleen alone (450 rad in 17 sessions and 28 days) the suppression of any hepatic myeloid metaplasia was observed simultaneously with the regression of myelemia and erythroblastemia and the drop in the number of circulating granulomonocytic stem cells. These observations allow to discuss the mode of action of the splenic radiotherapy and the relationship between myeloid metaplasia and the circulating hematopoietic cells (proliferating granulocytic and erythrocytic cells and stem cells).

Bone Marrow Cells↗
PubMed1979

Splenectomy in myeloid metaplasia.

Between 1960 and 1977, 50 patients with agnogenic myeloid metaplasia were splenectomized. Twenty-five of 26 patients with painful splenomegaly, 4 of 9 patients with refractory hemolytic anemia, 4 of 10 patients with refractory thrombocytopenia, and 4 of 4 patients with portal hypertension showed significant benefit from the procedure. There were five immediate postoperative deaths. Four of these deaths occurred early in our series of splectomies for myeloid metaplasia before 1970. Only one death has occurred in the last 21 patients operated on. Survival following splenectomy averaged 25.5 mo.

Female↗
PubMed1994

Post-polycythemia myeloid metaplasia: experience with a large cohort of patients.

The common origin of myeloproliferative disorders can explain the possible evolution of polycythemia vera to post-polycythemia myeloid metaplasia (PPMM). Such a possible event is usually considered linked to the use of myelosuppressive agents in particular 32P. Occasionally, myelofibrosis following essential thrombocythemia has also been described. We report here 19 cases of post-polycythemia myeloid metaplasia out of 214 polycythemia vera patients (8.8%). The majority of these patients received 32P therapy. However, busulfan also seems to have some role in the modification of polycythemia vera. In particular, the association of more than one myelosuppressive agent may favour the evolution of PPMM.

Adult↗
PubMed1994

p53 immunoreactivity in Barrett's metaplasia, dysplasia, and carcinoma.

Barrett's esophagus is a metaplastic condition with an unpredictable potential for neoplasia. Mutations of the tumor-suppressor gene p53 have been implicated in the evolution of some carcinomas. These mutations frequently result in intranuclear protein accumulation, which can be detected immunohistochemically. This study was undertaken to determine whether p53 immunoreactivity in Barrett's esophagus is a marker of neoplasia and, if so, when it occurs in the metaplasia-dysplasia-carcinoma sequence. Twenty-eight esophageal resection specimens were studied. Barrett's mucosa was present in each specimen, low-grade dysplasia in 27, high-grade dysplasia in 26, intramucosal cancer in 18, and submucosal cancer in 5. Immunohistochemical staining with the monoclonal antibody Pab1801 was used to detect the intranuclear protein product of mutated p53. No p53 immunoreactivity was seen in specimens of Barrett's mucosa or low-grade dysplasia. p53 immunoreactivity was found only in specimens of high-grade dysplasia, intramucosal cancer, and submucosal cancer. Sixty-nine percent (18/26) of these specimens exhibited mutated p53; 18 of 26 specimens of high-grade dysplasia (69%), 12 of 18 intramucosal cancer specimens (67%), and two of five submucosal cancer specimens (40%) expressed mutated p53. When p53 staining was observed, the spectrum of neoplastic changes (high-grade dysplasia, intramucosal cancer, submucosal cancer) within the specimen was positive. We conclude that (1) p53 immunoreactivity in Barrett's esophagus is a frequent, but not inclusive, marker for high-grade dysplasia, intramucosal cancer, and submucosal cancer and (2) immunoreactivity occurs late in the metaplasia-dysplasia-carcinoma sequence, during the transition to high-grade dysplasia.

Adenocarcinoma↗
PubMed1994

[Spontaneous infection of ascitic fluid as a form of presentation of agnogenic myeloid metaplasia].

In most cases, the clinical manifestation of the agnogenic myeloid metaplasia is an anemic syndrome. Ascitis secondary to portal hypertension as the first manifestations is a rare clinical condition. Finally, the form of presentation of the idiopathic rare. We present a case of agnogenic myeloid metaplasia in a 64 years-old patient whose form of presentation was an spontaneous infection of the ascitic fluid. In our review of the literature we have not found any other case with similar characteristics.

Ascitic Fluid↗
PubMed1997

Esophageal columnar metaplasia (Barrett's esophagus).

This article explores the historical roots for the present confusion regarding diagnostic criteria for Barrett's esophagus. The author recommends using an alternative classification system for the columnar-lined esophagus that does not rely solely on arbitrary and imprecise endoscopic landmarks and measurements. Endoscopic features that suggest the presence of intestinal metaplasia in the esophagus are discussed and illustrated. The role of endosonography and the endoscopic techniques for ablating the esophageal columnar lining also are considered. Finally, the author lists specific management recommendations for patients who have esophageal columnar metaplasia.

Adenocarcinoma↗
PubMed1979

Transient myeloid metaplasia associated with an unusual hemoglobin in a newborn infant.

A newborn infant presented with hepatosplenomegaly, rash, anemia, and leukocytosis at one day of age and manifested characteristic myeloid metaplasia by one mouth of life. Vitamin B12 and leukocyte alkaline phosphatase were elevated and platelet aggregation was impaired. Myelofibrosis was not present and neutrophil function was preserved. An unidentified high isoelectric point hemoglobin with unusual chromatographic and electrophoretic behaviors was found to comprise 12% of the total hemoglobin. The myeloid metaplasia and mutant hemoglobin disappeared over the subsequent months without biochemical or clinical residual. The available evidence was consistent with the mutant hemoglobin representing either a gamma chain or clonal embryonic chain variant. The inability to clarify prognostic factors in these unusual myeloproliferative syndromes suggests caution in the initiation of cytotoxic therapy.

Electrophoresis, Cellulose Acetate↗